Pigmentation disorders are disturbances of human skin color, either loss or reduction (depigmentation or hypopigmentation) which may be related to loss of melanocytes or to the inability of melanocytes to produce melanin or transport melanosomes correctly, or increase (hyperpigmentation) which is caused by an excessive production of melanin by melanocytes. Melanocytes are located at the lower layer (the stratum basale) of the skin's epidermis, the middle layer of the eye (the uvea), the inner ear, meninges, bones, and heart.
Vitiligo is an acquired depigmentation of the skin inducing a marked alteration of the quality of life of affected subjects. This disease is characterized by destruction of melanocytes that occurs mainly in the skin and results in the appearance of well circumscribed white macules. There are two types of vitiligo, i.e., segmental vitiligo located unilaterally on an area of the face, upper body, legs or arms, which in general does not change; and generalized vitiligo, which has more or less often bilateral symmetrical spots on areas of repeated friction or pressure and may become increasingly important over the years. The exact physiopathological mechanism that leads to the destruction of melanocytes is still elusive, and involves autoimmunity (Passeron T; Ortonne JP 2005; Spritz 2007).
Vitiligo is common and affects 1% to 2% of the general population. For many patients with vitiligo, the disfigurement caused by the disease has a great impact on their quality of life (Ongenae K et al. 2006).
Halting the disease progression and repigmenting the lesional skin represent the two faces of the therapeutic challenge in vitiligo. So far, none of them has been successfully addressed. Oxidative stress and immune system in genetically predisposed subjects participate to the complex pathophysiology of vitiligo.
Currently, there are several therapeutic modalities that can be proposed for the treatment of vitiligo. Treatments such as narrow-band UVB (Nb-UVB), excimer light, topical steroids, topical tacrolimus or pimecrolimus and combination approaches (with phototherapy and topical steroids or calcineurin inhibitors) can provide cosmetically acceptable repigmentation (>75%) [Lepe, 2003; Ostovari, 2004; Passeron, 2004; Taieb, 2013]. Unfortunately, repigmentation, consisting in vitiligo skin in the differentiation and proliferation of new melanocytes, remains difficult to achieve in most cases. Some localizations, such as hands and feet, are almost impossible to fully repigment with the current approaches. In addition, it is still very difficult to compare the efficacy of different treatment modalities and the results of different studies on the same treatment because: (i) most published studies are uncontrolled; and (ii) there is not a generally accepted biometric tool to assess disease severity and response to treatment. Recently, animal models using reactive T-cells against melanocyte antigens provided interesting data on the immune reaction potentially involved in the depigmentation of vitiligo skin but this model is not adapted to study mechanisms of melanocytes differentiation and repigmentation in vitiligo skin [Mosenson, 2013][Rashighi, 2014].
In the light of limited therapies and the lack of information about the physiopathology of hypopigmentation disorders such as vitiligo, there is a clear need for identifying new pharmacological markers allowing their correct and early diagnostic as well as their adequate management, and for new therapeutic targets allowing their prevention, attenuation or treatment.